Abstract
Mitochondrial Carrier Homolog 2 (MTCH2) is a novel regulator of mitochondria metabolism, which was recently associated with Alzheimer's disease. Here we demonstrate that deletion of forebrain MTCH2 increases mitochondria and whole-body energy metabolism, increases locomotor activity, but impairs motor coordination and balance. Importantly, mice deficient in forebrain MTCH2 display a deficit in hippocampus-dependent cognitive functions, including spatial memory, long term potentiation (LTP) and rates of spontaneous excitatory synaptic currents. Moreover, MTCH2-deficient hippocampal neurons display a deficit in mitochondria motility and calcium handling. Thus, MTCH2 is a critical player in neuronal cell biology, controlling mitochondria metabolism, motility and calcium buffering to regulate hippocampal-dependent cognitive functions.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Animals
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Calcium / metabolism*
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Cognition / physiology*
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Energy Metabolism / physiology
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Female
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Hippocampus / metabolism*
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Hippocampus / physiopathology
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Locomotion / physiology
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Long-Term Potentiation / physiology
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Male
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Maze Learning / physiology
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Mice
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Mice, Knockout
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Mitochondria / genetics
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Mitochondria / metabolism*
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Mitochondria / pathology
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Mitochondrial Membrane Transport Proteins / deficiency
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Mitochondrial Membrane Transport Proteins / genetics*
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Neurons / metabolism*
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Neurons / pathology
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Postural Balance / physiology
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Prosencephalon / metabolism
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Prosencephalon / physiopathology
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Psychomotor Disorders / metabolism
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Psychomotor Disorders / physiopathology
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Rotarod Performance Test
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Spatial Memory / physiology
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Synaptic Transmission / physiology
Substances
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Mitochondrial Membrane Transport Proteins
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Mtch2 protein, mouse
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Calcium